RESUMO
BACKGROUND: Clinical reports indicate that spinal cord injury (SCI) initiates profound gastric dysfunction. Gastric reflexes involve stimulation of sensory vagal fibers, which engage brainstem circuits that modulate efferent output back to the stomach, thereby completing the vago-vagal reflex. Our recent studies in a rodent model of experimental high thoracic (T3-) SCI suggest that reduced vagal afferent sensitivity to gastrointestinal (GI) stimuli may be responsible for diminished gastric function. Nevertheless, derangements in efferent signals from the dorsal motor nucleus of the vagus (DMV) to the stomach may also account for reduced motility. METHODS: We assessed the anatomical, neurophysiological, and functional integrity of gastric-projecting DMV neurons in T3-SCI rats using: (i) retrograde labeling of gastric-projecting DMV neurons; (ii) whole cell recordings from gastric-projecting neurons of the DMV; and, (iii) in vivo measurements of gastric contractions following unilateral microinjection of thyrotropin-releasing hormone (TRH) into the DMV. KEY RESULTS: Immunohistochemical analysis of gastric-projecting DMV neurons demonstrated no difference between control and T3-SCI rats. Whole cell in vitro recordings showed no alteration in DMV membrane properties and the neuronal morphology of these same, neurobiotin-labeled, DMV neurons were unchanged after T3-SCI with regard to cell size and dendritic arborization. Central microinjection of TRH induced a significant facilitation of gastric contractions in both control and T3-SCI rats and there were no significant dose-dependent differences between groups. CONCLUSIONS & INFERENCES: Our data suggest that the acute, 3 day to 1 week post-SCI, dysfunction of vagally mediated gastric reflexes do not include derangements in the efferent DMV motoneurons.
Assuntos
Tronco Encefálico/fisiologia , Motilidade Gastrointestinal/fisiologia , Neurônios Motores/fisiologia , Traumatismos da Medula Espinal/fisiopatologia , Estômago/inervação , Animais , Modelos Animais de Doenças , Imuno-Histoquímica , Masculino , Neurônios Motores/patologia , Neurônios Aferentes/patologia , Neurônios Aferentes/fisiologia , Técnicas de Patch-Clamp , Ratos , Ratos Wistar , Vértebras Torácicas , Nervo Vago/patologia , Nervo Vago/fisiologiaRESUMO
BACKGROUND: Vagally dependent gastric reflexes are mediated through vagal afferent fibers synapsing upon neurons of the nucleus tractus solitarius (NTS) which, in turn modulate the preganglionic parasympathetic dorsal motor nucleus of the vagus (DMV) neurons within the medullary dorsal vagal complex (DVC). The expression and transport of ghrelin receptors has been documented for the afferent vagus nerve, and functional studies have confirmed that vagal pathways are integral to ghrelin-induced stimulation of gastric motility. However, the central actions of ghrelin within the DVC have not been explored fully. METHODS: We assessed the responses to ghrelin in fasted rats using: (i) in vivo measurements of gastric tone and motility following IVth ventricle application or unilateral microinjection of ghrelin into the DVC and (ii) whole cell recordings from gastric-projecting neurons of the DMV. KEY RESULTS: (i) IVth ventricle application or unilateral microinjection of ghrelin into the DVC-elicited contractions of the gastric corpus via excitation of a vagal cholinergic efferent pathway and (ii) ghrelin facilitates excitatory, but not inhibitory, presynaptic transmission to DMV neurons. CONCLUSIONS & INFERENCES: Our data indicate that ghrelin acts centrally by activating excitatory synaptic inputs onto DMV neurons, resulting in increased cholinergic drive by way of vagal motor innervation to the stomach.
Assuntos
Motilidade Gastrointestinal/efeitos dos fármacos , Grelina/farmacologia , Bulbo/efeitos dos fármacos , Nervo Vago/efeitos dos fármacos , Animais , Motilidade Gastrointestinal/fisiologia , Masculino , Bulbo/fisiologia , Neurônios/efeitos dos fármacos , Neurônios/fisiologia , Ratos , Ratos Long-Evans , Potenciais Sinápticos/efeitos dos fármacos , Nervo Vago/fisiologiaRESUMO
Injury prevention can be achieved, but it will require a fundamental reexamination of our approach to injury causation. We must learn to examine the manufacturing and marketing practices of companies that produce the products associated with children's injuries, for these are the real culprits in our national childhood injury plague. Most importantly, we must learn to demand from industry that it take injury prevention seriously. If it refuses to do so it must face the consequences before the American system of justice. Legal advocacy can be a valuable tool in this effort. The legal system provides the means to pierce the corporate veil of secrecy and to learn how and why products are made of hazardous design. Under the light of public scrutiny, culprit companies can be made to pay the price for producing hazardous products. Only in this manner will industry be given the incentive to increase product safety.
Assuntos
Defesa da Criança e do Adolescente/legislação & jurisprudência , Legislação como Assunto , Jogos e Brinquedos , Ferimentos e Lesões/prevenção & controle , Criança , Prova Pericial , Humanos , Papel do Médico , Segurança , Estados UnidosRESUMO
An incarcerated gravid uterus is a dangerous but fortunately infrequent complication of pregnancy. Many sequelae may result from this condition. The purpose of this paper is to present an unusual complication after repositioning of the gravid uterus and to discuss management of the incarcerated uterus in pregnancy.